T cell activation induces CuZn superoxide dismutase (SOD)-1 intracellular re-localization, production and secretion.

摘要: Abstract Reactive oxygen species (ROS) behave as second messengers in signal transduction for a series of receptor/ligand interactions. A major regulatory role is played by hydrogen peroxide (H2O2), more stable and able to freely diffuse through cell membranes. Copper–zinc superoxide dismutase (CuZn-SOD)-1 cytosolic enzyme involved scavenging radicals H2O2 molecular oxygen, thus representing source peroxides. Previous studies suggested that anion generation are T receptor (TCR)-dependent signaling. Here, we describe antigen-dependent activation human lymphocytes significantly increased extracellular SOD-1 levels lymphocyte cultures. This effect was accompanied the synthesis SOD-1-specific mRNA induction microvesicle secretion. It note its concentration specifically population, while no significant changes were observed “non-T” counterpart. Moreover, confocal microscopy showed modify intracellular localization cells. Indeed, clear recruitment TCR clusters. The ROS scavenger N-acetylcysteine (NAC) inhibited this phenomenon. Further needed define whether SOD-1-dependent superoxide/peroxide balance relevant regulation activation, well functional cross talk between immune effectors.